The research presented here addresses the role of the central dopamine system in endogenous pain modulation as it pertains to sensitivity to noxious stimuli, and the capacity to engage antinociceptive resources following administration of placebo analgesic. Based on substantial data from the animal literature and converging evidence from both clinical samples and healthy human volunteers, it is proposed that D2- like dopamine receptor density in neural components of the primary dopaminergic reward pathway is differentially associated with these modulatory capacities. It is also proposed that beliefs regarding magnitude and probability of receiving a purportedly active analgesic will affect the relationship between placebo response and D2 dopamine receptor density. The proposed study will test whether baseline pain sensitivity and placebo analgesia when there is a high or low probability of receiving a purportedly active treatment are associated with D2/D3 dopamine receptor availability in striatal and extrastriatal brain regions as measured with [18F]fallypride PET. [unreadable] [unreadable] [unreadable]